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Abusive Head Trauma Shaken Baby Syndrome

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Abusive Head Trauma Shaken Baby Syndrome Powered By Docstoc
					Parental Substance Abuse and
 Drug Endangered Children

     Walter F. Lambert, MD
      University of Miami
     Child Protection Team
Parent Produced Stressors
   Low self-esteem
   Unmet emotional needs
   Abused as a child
   Depression
   Substance abuse
   Personality disorder or psychiatric illness
   Ignorance of child rearing-unrealistic
    expectations
   Teenage pregnancy
Triggering Situations

 Discipline
 Argument/family conflict

 Substance Abuse

 Acute environmental problem
Drugs of Abuse
 Alcohol
 Tobacco

 Marijuana

 Heroin/Methadone

 Cocaine

 Methamphetamine
Concepts
 Exposure
 Addiction

 Direct effects on
  fetus/infant/child/adolescent
 Effects of parental substance
  abuse
 Reporting to CPS
Drug Endangered Children
 Shift in paradigm
 Sensationalism

 Treatment

 Effect of ASFA on case
  plans
Fetal Alcohol Syndrome
   Approximately 10% of women in
    childbearing years are problem drinkers
    (up to 6-7 drinks per day)
   Alcohol is probably the most common
    teratogen ingested during pregnancy
    and most common identifiable cause of
    intellectual disability (mental
    retardation)
Acute Perinatal
  Alcohol Intoxication
   Women who are acutely intoxicated may
    deliver infant who smells of alcohol, has
    blood alcohol level in the cord blood, has
    signs/symptoms of intoxication with CNS
    depression and hypoglycemia
   Some infants born to mothers who chronically
    abuse alcohol may present with withdrawal
    symptoms (tremors, wakefulness and
    restlessness, excessive crying, hypertonia,
    and excessive startling; persist for 72 hours
Fetal Alcohol Syndrome
   Constellation of physical, behavioral and
    cognitive abnormalities
   Criteria: specifc craniofacial dysmorphic
    features, prenatal or postnatal growth
    deficiency, central nervous system
    neurodevelopmental findings
Fetal Alcohol Syndrome
   Diagnosis requires a history of maternal
    alcohol use (proven or presumed) and
    elements of the three primary
    diagnostic categories
   Partial FAS: confirmed facial anomalies
    and either growth retardation or CNS
    involvement or other unexplained
    behavior abnormalities
Fetal Alcohol Syndrome
   Characteristic facial anomalies
       Short palpebral fissures
       Ptosis
       Flat midface
       Upturned nose
       Smooth philtrum
       Thin upper lip
Fetal Alcohol Syndrome
   Growth Retardation
       Low relative birth weight
       Growth failure despite adequate nutrition
       Low weight relative to height
        Fetal Alcohol Syndrome
   CNS neurodevelopmental findings
       Microcephaly
       Structural brain abnormalities (agenesis of the
        corpus callosum and cerebellar hypoplasia
       Other neurological signs (fine motor difficulties,
        sensorineural hearing loss, poor gait
        coordination, and poor eye-hand coordination
Fetal Alcohol Syndrome
   Unexplained behavioral abnormalities
       Learning difficulties
       Poor school performance
       Poor impulse control
       Problems with social perception
       Poor language abilities
       Poor math skills
       Impaired memory and judgement
Fetal Alcohol Syndrome
   Birth defects
       Congenital heart defects
       Skeletal and limb deformities
       Anatomic renal abnormalities
       Ophthalmologic abnormalities
       Hearing loss
       Cleft lip or palate
Classification of alcohol-related effects


   Fetal alcohol syndrome
   Partial FAS
   Alcohol-related birth defects (ARBD)
   Alcohol-related neurodevelopmental
    disorder (ARND)
Fetal Alcohol Syndrome
   Etiology:
       Infrequent binge drinking with occasional
        high blood alcohol levels
       Mild-to-moderate regular drinking with
        lower peak blood alcohol levels but more
        continuous fetal exposure
        Fetal Alcohol Syndrome
   Pathogenesis:
       Exposure of the developing fetus to toxic
        levels of alcohol and its metabolites
       Exposure in the 1st trimester affects
        organogenesis and craniofacial development
       Continuing use in later preganancy results in
        low birth weight and affects postnatal growth
       Brain development begins in early pregnancy
        and undergoes growth spurt with maturation
        of neurons in second and third trimester
       Tobacco
   Although prevalence of smoking in US has
    decreased, up to 20% of pregnant women continue
    to smoke throughout gestation.
   No documented increased risk of birth defects
   Major impact is decreased birth weight
   Prenatal (and postnatal) smoking is risk factor for
    SIDS
   Secondhand smoke associated with increased risk
    of respiratory disease
        Marijuana
   Concern due to fact that marijuana is lipid-soluble
    and concentrates in fatty tissues (brain)
   Older studies did not address long-term issues
   Marijuana today much more potent
   Anecdotal reports of prenatal marijuana-exposed
    children with normal IQ, but specific learning
    disabilities
   Cannabis withdrawal syndrome
      Heroin
   IV use
   Recent cultivation in Colombia and Mexico:
    ability to snort or smoke
   Physical dependence of user and neonate
   Need to wean infant with use of
    phenobarbital
   Methadone withdrawal longer then heroin
Cocaine
   Cocaine powder vs. crack
   Intensely stimulates brain’s pleasure
    centers (not just “buzz”, but euphoria)
   “highly addictive”: 16% of people who
    try cocaine become “hooked”
   Binging
         Cocaine
   Prenatal effects
   Prematurity is greatest risk
   No perinatal withdrawal syndrome
   Post-natal behavior of the drug using parent
    has greatest effect
       Binging
       Neglect (physical and emotional)
       Economic
       Criminal and violence exposure
         Methamphetamine:
        Historical Background
   1887: Amphetamine first synthesized
   1932: Benzathine nasal spray for
    asthma and rhinitis
   1937: Amphetamine tablet for
    narcolepsy. A report that year states
    that intellectual performance can be
    enhanced via increased wakefulness
   1930’s and 40’s: Abuse of
    methamphetamine in US and abroad
Methamphetamine Clan Lab
Methamphetamine Clan Lab
     Methamphetamine: Crank
   Originally transported across the
    country in the crank cases of
    motorcycles by biker gangs
   Methamphetamine manufacturing:
    Large “plants” in California
    “Mom & Pop” type spreading from
    West & Midwest into East Coast and
    Florida
         Chemical Properties
   N-methyl homologue of amphetamine
   White, odorless, bitter crystalline
    powder
   Color varies with manufacturing process
   Street names: pink, quartz, peanut
    butter speed, crank, tweak, go
            The Effects of
          Methamphetamine
   The drug acts on the body in 2 main
    areas:
   Peripherally: Your blood pressure,
    heart rate, pupil size
   Centrally: Your brain function
   Some users binge then crash
   Others are “weekend” users
Peripheral Effects in Users
The mechanism appears to be
 methamphetamine’s ability to
 stimulate release of norepinephrine at
 nerve terminals and of epinephrine
 from the adrenal medulla and include
 tachycardia, tachypnea, hypertension,
 dry mouth, mydriaisis and blurry
 vision.
             Pharmacology
   The N-methyl group that differentiates
    amphetamine from methamphetamine
    decreases the polarity of the molecule
    and allows for better penetration of the
    blood-brain barrier
   Half-life ranges from 10-30 hours
    depending on dosage, form, and
    urinary pH
            Pharmacology
   At the cellular level, dopamine is
    displaced from specific nerve
    terminals, causing hyperstimulation
    of dopaminergic receptor neurons
    in the synaptic cleft
   Damage is probably due to excess
    dopamine
   Crash is from dopamine depletion
Acute Central Effects in Users
   Irritability, impulsivity, impaired
    judgment, insomnia, and psychotic
    behaviors such as hallucinations
    and paranoia
   Methamphetamine can both induce
    an acute toxic psychosis in
    previously healthy persons and
    precipitate a psychotic episode in
    those with psychiatric illnesses
        Chronic Central Effects in Users
   Compulsive or repetitive behaviors are
    manifestations of chronic use. Long
    term use in humans has resulted in
    delusional, paranoid behavior, psychosis
    and violence. The distinguishing feature
    of the psychosis is its visual or tactile
    hallucinations, as opposed to generally
    auditory hallucinations in schizophrenia
    Chronic Central Effects in Users
   CNS “kindling” phenomenon:
   Patients who have used amphetamines
    over a long period, especially those who
    have had psychotic episodes from its
    use, may be pushed into a frank
    psychosis by even very small amounts
    of an amphetamine, or by any stimulant
    including caffeine or nicotine
              Chronic Use
   Tolerance: The chronic user will
    progressively increase the dose to
    obtain desired effects
   Methamphetamine abusers may
    increase their dose 50 to 100 times the
    initial amount over time: up to several
    hundred milligrams/day, which would
    be fatal to the non-user
    Chronic Central Effects in Users
   Physical detoxification can take weeks,
    while psychological detoxification can
    take months.
   Unless injecting, it is possible for
    individuals to take methamphetamine
    for a period of years before intolerable
    negative consequences of the drug
    begin to occur.
    Potential Chemical Toxicities
   When a clandestine lab is raided, the team
    wears special protective gear that can weigh
    up to 30-40 pounds
   The most significant health risk related to the
    production of meth is the acute injury
    secondary to massive chemical exposure via
    inhalation or contact to the skin and eyes
   The manufacture of 1 pound of meth can
    produce 5-6 pounds of toxic waste
    Potential Chemical Toxicities
   These can be corrosive, explosive,
    flammable, and toxic.
   Exposure can occur via skin absorption,
    inhalation, ingestion, or injection.
   The labs can be booby-trapped: A light
    bulb can be filled with ether so that the
    mere act of turning on its light switch
    causes enough friction to cause an
    explosion.
           Reported Toxicities
   JAMA 12/6/00: events reported to the
    Hazardous Substances Emergency Events
    Surveillance system from 1996-1999 noted
    112 methamphetamine-associated events
    with 155 persons injured.
   51 % were first responders: police officers,
    EMTs, firefighters, and hospital employees.
    54.1 % had respiratory irritation (cough),
    difficulty breathing, throat irritation
   10.8 % had eye irritation.
     What about the Children?
   Children breathe faster than adults
   Children have a faster heart beat than
    adults
   Children are smaller and closer to the
    ground than adults
   Just imagine their side effects
   They have a heavier exposure to the
    chemicals due to the above
     What about the Children?
   Their nervous system is still
    developing
   The food they eat is on the same
    counter as the meth lab
   The food in the refrigerator is near
    the chemicals: meth has been
    analyzed from food taken from clan
    meth labs
     What about the Children?
   Children removed from meth labs have
    had their urine test positive for
    methamphetamine
   They may have been exposed to the
    vapors and inhaled it
   They may have eaten it or drank it
    unknowingly
      Preliminary Data: Tulsa
      DEC Nurses & Justice Center
   55 children examined Jan 00 - Mar 02
   Majority of children filthy:
   33/55 had either an abnormal physical
    exam or evidence of neglect
   Developmental delays common,
    especially speech-language delays: 6/55
    ages 4-5 years old
    No consistent abnormal bloodwork
         Testing for drugs of abuse
   Screening tests: (high sensitivity)
       thin-layer chromatography/immunoassay
       Inexpensive but influenced by adulterants
       Used in emergency and substance abuse
        treatment
   Confirmatory tests: (high specificity)
       Gas chromatography/mass spectrometry
       Expensive but accurate
        Drug testing
   Approximate duration of detection in urine:
       Amphetamines:              2 days
       Cannabinoids-single use:   3 days
         moderate use (3x/week):   5 days
         heavy use (6x/week):      10 days
         chronic heavy use:        21-27 days
       Cocaine metabolites:       2-3 days
       Methamphetamine:           2 days
    Medical Evaluation Protocol
   Urine for methamphetamines and
    other drugs of abuse (“toxicology screen”)
    should be obtained as quickly as possible;
    clean catch or bag, preferably within 2 hours,
    but up to 12, of removal from scene via
    chain of evidence. If need be, the urine can
    be refrigerated over night and sent the next
    morning. Notify lab that will be performing
    the assay to identify ANY DETECTABLE LEVEL
    of drug, not to use the industrial cut-off.
Children Are Our Future